New Computerized Planning Algorithm and Clinical Testing of Optimized Nuss Bar Design for Patients with Pectus Excavatum.

BACKGROUND Computer-aided design (CAD) has been used in the Nuss procedure to determine the bar length and shape. Despite computer aid, the shape and design remain quite intuitive. We tested a new algorithm to determine the optimal bar shape. MATERIAL AND METHODS The normal sterno-vertebral distance was defined on computed tomography (CT) scans of patients without pectus excavatum (PEx) at the same level where the deepest depression was found on CT scans of 97 patients with PEx. Four points were marked on the CT scan of 60 patients with PEx at the deepest deformity: P1: edge of the vertebra; P2: edge of the deformity; P3: the expected contact point of the bar and the rib; and P4: the expected end of the bar. The algorithm generated 3 circles upon these points, and the fusion of the arcs drew the line of the ideal bar. Corrected and normal sterno-vertebral distance values were compared with the Mann-Whitney U test. Ten bars were bent manually guided by a 1: 1 printout of the designed bar and were implanted in 10 adolescents. RESULTS The shortest sterno-vertebral distance was 3 cm below the intermammillary line in PEx patients. The normal mean sterno-vertebral distance at this level was 10.16±1.35 cm in non-PEx patients. The mean virtually corrected sterno-vertebral distance was 10.28±1.27 cm. No significant difference was found (P=0.44). The bars were seamless and were successfully implanted. No bar needed adjustment, the operation time was shorter, and the patient satisfaction score was 9.4/10. CONCLUSIONS With our new algorithm, an optimal Nuss bar can be designed.

Curcumin mitigates ochratoxin A-induced oxidative stress and alters gene expression in broiler chicken liver and kidney.

The study aimed to evaluate the effect of curcumin (CURC) supplementation on broiler chickens exposed to ochratoxin A (OTA), by examining biochemical parameters and the expression of glutathione redox system genes and their regulation. OTA reduced glutathione content in the liver while increasing glutathione peroxidase activity. CURC showed no significant effects. Kidney parameters remained mostly unaffected. Gene expression analysis revealed OTA-induced upregulation of KEAP1, NRF2, AHR, GPx4 and GSR genes in the liver. CURC supplementation led to the upregulation of GPx4 and AHR genes with OTA+CURC treatment, resulting in the downregulation of GPx4, KEAP1, NRF2 and AHR genes compared to OTA treatment alone. In the kidney, GPx4 was downregulated, and NRF2 and AHR were upregulated as an effect of OTA, while CURC upregulated the NRF2 gene only. OTA+CURC treatment led to the downregulation of GPx4, GSS and AHR genes compared to the control and downregulation of NRF2 and AHR genes compared to OTA. The results suggested that CURC is partly effective against OTA-induced oxidative stress and that the effect of OTA and CURC on the antioxidant response is regulated through the KEAP1-NRF2-ARE and AHR pathways.

Role of the glutathione redox system in the susceptibility of pheasants (Phasianus colchicus) to ochratoxin A.

The purpose of the present study was to investigate the effects of different dietary concentrations of ochratoxin A (OTA) on the growth, feed intake, mortality, blood plasma protein content and some parameters of lipid peroxidation and the glutathione redox system of pheasant chicks in a three-week long trial. A total of 320 seven-day-old female pheasants were randomly assigned to four treatment groups (n = 40 in each), fed with a diet artificially contaminated with OTA [control (<0.02 mg/kg), 0.88 mg/kg, 1.14 mg/kg and 1.51 mg/kg] for 21 days (up to 28 days of age). The pheasant chicks were sacrificed at early (12, 24 and 72 h) and late (7, 14 and 21 days) stages of mycotoxin exposure to check the effect of OTA. Minimal feed refusal was found in the medium- and high-dose toxin groups (-9.8 and -7.9%, respectively), and body weight gain was nearly the same in all groups. The glutathione redox system was activated mainly in the liver, confirmed by significantly increased reduced glutathione content and glutathione peroxidase activity during the late phase of mycotoxin exposure and at a high-dose treatment. The results suggest that pheasants have low susceptibility to OTA, and activation of the glutathione redox system has importance in this tolerance.

Modification of the effects of aflatoxin B1 on the glutathione system and its regulatory genes by zeolite.

The purpose of the present study was to use oxidative stress markers for investigating the effect of zeolite (315 mg/kg of complete feed) in the case of aflatoxin B1 contamination (92 µg/kg complete feed). In a 21-day feeding trial with broiler chickens, oxidative stress parameters such as conjugated dienes, conjugated trienes, malondialdehyde, reduced glutathione content and glutathione peroxidase activity were not changed significantly by supplementation with this mycotoxin absorbent. The relative gene expression of transcription factors KEAP1 and NRF2 was not modified by the absorbent either. Still, the expression of GSS, GSR and GPX4 genes increased significantly due to the aluminosilicate supplementation. The results suggest that zeolite reduced lipid peroxidation in the blood plasma but not in the red blood cell haemolysate or the kidney. The relative expression of the genes encoding the glutathione redox system also changed as a result of zeolite supplementation, but these changes were not found at the protein level.

Combined effects of aflatoxin B1 and deoxynivalenol on the expression of glutathione redox system regulatory genes in common carp.

The purpose of the present study was to evaluate the short-term effects of aflatoxin B1 (AFB1 ) and deoxynivalenol (DON) exposure on the expression of the genes encoding the glutathione redox system glutathione peroxidase 4a (gpx4a), glutathione peroxidase 4b (gpx4b), glutathione synthetase (gss) and glutathione reductase (gsr) and the oxidative stress response-related transcription factors Kelch-like ECH-associated protein 1 (keap1) and nuclear factor-erythroid 2 p45-related factor 2 (nrf2) in liver, kidney and spleen of common carp. During the 24-hr long experiment, three different doses (5 µg AFB1 and 110 µg DON; 7.5 µg AFB1 and 165 µg DON or 10 µg AFB1 and 220 µg DON/kg bw) were used. The results indicated that the co-exposure of AFB1 and DON initiated free radical formation in liver, kidney and spleen, which was suggested by the increase in Nrf2 dependent genes, namely gpx4a, gpx4b, gss and gsr. Expression of keap1 gene showed upregulation after 8 hr of mycotoxin exposure, and also upregulation of nrf2 gene was found in kidney after 8 hr of exposure, while in the liver, only slight differences were observed. The changes in the expression of the analysed genes suggest that level of reactive oxygen species reached a critical level where other signalling pathway was activated as described by the hierarchical model of oxidative stress.

Short-term effects of deoxynivalenol, T-2 toxin, fumonisin B1 or ochratoxin on lipid peroxidation and glutathione redox system and its regulatory genes in common carp (Cyprinus carpio L.) liver.

The effects of a single oral dose of 1.82 mg kg-1 bw of T-2 and HT-2 toxin (T-2), 1.75 mg kg-1 bw deoxynivalenol (DON) and 15-acetyl DON, 1.96 mg kg-1 bw fumonisin B1 (FB1) or 1.85 mg kg-1 bw ochratoxin A (OTA) were investigated in common carp juveniles on lipid peroxidation, the parameters of the glutathione redox system including the expression of their encoding genes in a short-term (24 h) experiment. Markers of the initiation phase of lipid peroxidation, conjugated dienes, and trienes, were slightly affected by DON and OTA treatment at 16-h sampling. The termination marker, malondialdehyde, concentration increased only as an effect of FB1. Glutathione content and glutathione peroxidase activity showed significantly higher levels in the T-2 and FB1 groups at 8 h, and in the DON and FB1 groups at 16 h. The expression of glutathione peroxidase genes (gpx4a, gpx4b) showed a dual response. Downregulation of gpxa was observed at 8 h, as the effect of DON, FB1, and OTA, but an upregulation in the T-2 group. At 16 h gpx4a upregulated as an effect of DON, T-2, and FB1, and at 24 h in the DON and T-2 groups. Expression of gpx4b downregulated at 8 h, except in the T-2 group, and upregulation observed as an effect of T-2 at 24 h. The lack of an increase in the expression of nrf2, except as the effect of DON at 8 h, and a decrease in the keap1 expression suggests that the antioxidant defence system was activated at gene and protein levels through Keap1-Nrf2 independent pathways.

Interaction between the three frequently co-occurring Fusarium mycotoxins in rats.

To test the complex, acute biochemical effects of combined, naturally co-occurring fusariotoxins, a 5-day rat study was performed. Mycotoxin treatment was invented by intraperitoneal injection: FB1 (F): 9 µg/animal/day (approx. 30 µg/kg bw/day), DON (D): 16.5 µg/animal/day (approx. 55 µg/kg bw/day) and ZEN (Z): 12.75 µg/animal/day (approx. 42.5 µg/kg bw/day). The binary groups (FB1 and DON [FD], FB1 and ZEN [FZ] and DON and ZEN [DZ]) as well as the ternary (FB1 , DON and ZEN [FDZ]) group were dosed at the same combined level as the individual mycotoxins. Body weight, feed intake and mortality were not affected by any of the treatments. FB1 and DON in combination (FD) increased the plasma aspartate aminotransferase activity synergistically (compared to the individual FB1 and DON). In the liver, both the total glutathione (GSH) and the glutathione peroxidase (GPx) activity were increased (p < 0.05) by the binary FB1 and ZEN (FZ) and the DON and ZEN (DZ) groups as well as the ternary FB1 , DON and ZEA group (FDZ) compared to the control. The GSH level of the ternary group was significantly increased compared to the FB1 group, whereas the GPx activity of the ternary group was significantly increased compared to all three the individual mycotoxin groups. The Bliss independence method revealed synergism between DON and ZEN (DZ), as well as FB1 and DON (FD) on liver GPx activity. None of the toxins alone or in combination exerted strong genotoxicity on lymphocytes, neither on the gross histopathological characteristics. However, even at these low levels acute exposure of more than one of these mycotoxins (FB1 , DON and ZEN) affected metabolic and detoxification changes.

Fumonisin B1 exposure increases Hsp70 expression in the lung and kidney of rats without inducing significant oxidative stress.

The objective of this experiment was to determine whether fumonisin B1 (FB1) added to the diet of rats in a dose of 50 mg/kg changes the production of heat shock protein 70 (Hsp70) in the lungs and kidney of rats. We also studied the effect of this mycotoxin on the antioxidant system of the body. Mature (8 weeks old) male Wistar Crl:WI BR rats (n = 6/group) were fed the toxin-containing diet for 5 days. FB1 resulted in a 7% body weight reduction without significantly changing the feed intake. Western blot analysis of the lungs and kidney demonstrated a substantial (1.4-fold and 1.8-fold, respectively) increase in Hsp70 expression. Alterations could not be detected in the clinical chemical parameters (total protein, albumin, total cholesterol, glucose, creatinine and urea concentrations, and aspartate aminotransferase activity). There was no statistically significant change in malondialdehyde concentrations and the measured antioxidant parameters (the amount of reduced glutathione, GSH and glutathione peroxidase activity, GPx) in the blood plasma, lung and kidney tissue. Thus, it can be concluded that FB1 did not induce oxidative stress in the lungs and kidney, but increased Hsp70 production.

Short-term effects of T-2 toxin or deoxynivalenol on glutathione status and expression of its regulatory genes in chicken.

Short-term (48-hour) effects of 3.74/1.26 mg kg-1 T-2/HT-2 toxin or 16.12 mg kg-1 DON in feed were investigated in the liver of three-week-old cockerels (body weight: 749.60 ± 90.98 g). Markers of lipid peroxidation showed no significant changes. At hour 24, glutathione content in the T-2/HT-2 toxin group was significantly higher than in the control. Glutathione peroxidase activity was significantly higher than the control at hour 24 in the T-2/H-2 toxin group and at hour 48 in the DON group. In the DON group, expression of the glutathione peroxidase 4 gene (GPX4) was significantly lower than in the control at hours 12 and 14, and higher at hour 48. Expression of the glutathione reductase gene (GSR) was significantly lower than in the control at hour 12 in the T-2/HT-2 toxin group, and at hours 12, 24 and 48 in the DON group. However, at hour 36 higher GSR expression was measured in the DON group. Due to the effect of both trichothecenes, expression of the glutathione synthetase gene (GSS) was significantly lower than in the control at hours 24 and 48. In conclusion, T-2/HT-2 toxin and DON had a moderate short-term effect on free radical formation. T-2/HT-2 toxin induced more pronounced activation of the glutathione redox system than did DON.

Short-term effects of T-2 toxin or deoxynivalenol on lipid peroxidation and the glutathione system in common carp.

The purpose of this study was to investigate the short-term effects of a single oral dose of T-2 and HT-2 toxin at 0.15, 0.33 and 1.82 mg kg-1 body weight, or deoxynivalenol (DON) and 15-acetyl-DON at 0.13, 0.31 and 1.75 mg kg-1 body weight in common carp. Conjugated dienes and trienes (the early markers of lipid peroxidation) were elevated in all DON-treated groups at the 16th hour, while thiobarbituric acid reactive substances (TBARS; termination marker) were increased at the highest dose of DON at the 16th and 24th hours. T-2 toxin did not cause changes in these parameters. Glutathione content and glutathione peroxidase activity showed higher levels at the 16th hour as the effect of both mycotoxins. The expression of glutathione peroxidase (GPx4) genes (gpx4a and gpx4b) revealed a dual response. Downregulation was observed at the 8th hour, followed by an induction at the 16th hour, at the lowest dose of both mycotoxins. Higher doses revealed long-drawn emergence and an elevation was observed only at the 24th hour. However, at the lowest and highest doses of DON or T-2 toxin the changes in gene expression were delayed, which may be related to the low oxidative stress response, as suggested by the expression profiles of the nrf2, keap1, gpx4a and gpx4b genes.

Effects of subclinical Mycobacterium avium ssp. paratuberculosis infection on some physiological parameters, health status and production in dairy cows.

Milk yield, milk ingredients, health and other, production-related parameters of subclinically infected, Mycobacterium avium ssp. paratuberculosis (MAP-) shedding (positive faecal PCR, n = 20) and non-shedding (negative faecal PCR, n = 10) dairy cows were compared in the period from 10 days prepartum to 120 days postpartum. Body condition, rumen fill and faeces scores were lower in the MAP-shedding cows. There was no significant difference in plasma or urine metabolic parameters between the groups. Milk yield and lactose content tended to be lower (P = 0.074 and 0.077, respectively), somatic cell count tended to be higher (P = 0.097), while milk fat content was significantly higher (P = 0.006) in MAP-shedding cows than in the controls. Milk protein content did not differ between the groups. All other health and production parameters [number of reproductive tract treatments, number of udder treatments, number of artificial inseminations (AIs), calving interval, and service period] were significantly better in the control group. It is concluded that MAP infection, even in a subclinical form, has a significant impact on some production and health parameters of dairy cows.

Multi-Fusarium mycotoxin exposure activates Nrf2 and Ahr pathway in the liver of laying hens.

This study investigates gene expression changes in laying hens exposed to trichothecene mycotoxins, known to induce oxidative stress and affect xenobiotic transformation and antioxidants. A 3-day feeding trial tested low and high doses of T-2/HT-2 toxin, DON/3-AcDON/15-AcDON, and FB1 in hen feed. Results showed increased expression of AHR, AHRR, HSP90, and CYP1A2 genes on days 2 and 3, suggesting a response to mycotoxin exposure. High doses down-regulated CYP1A2, AHR, and AHRR on day 1. KEAP1 expression decreased on day 1 but increased dose-dependently on days 2 and 3. NRF2 was up-regulated by low and down-regulated by high doses on day 1, then increased on days 2 and 3. Antioxidant-related genes (GPX3, GPX4, GSS, GSR) showed dose-dependent responses. Low doses up-regulated GPX3 and GPX4 throughout, while high doses up-regulated GPX3 on days 2 and 3 and GPX4 on day 3. GSS was up-regulated on day 3. Results indicate that toxic metabolites formed by phase I biotransformation rapidly induce ROS formation at low doses through the AHR/Hsp90/CYP1A2 pathway at the gene expression level, but at high levels, ROS-induced oxidative stress manifests later. Study showed simultaneous activation of redox-sensitive pathways: aryl hydrocarbon receptor (Ahr) and nuclear factor erythroid-derived 2-like 2 (Nrf2) by multi-mycotoxin exposure.

Effect of aflatoxin B1 and sterigmatocystin on DNA repair genes in common carp.

The present study aimed to investigate the short-time (24 h) effect of aflatoxin B1 (AFB1) and sterigmatocystin (STC) on the expression of hsp70, p53, gadd45, and ogg1 genes in common carp hepatopancreas. Our results showed that aflatoxin B1 and sterigmatocystin can stimulate the expression of DNA repair genes, mainly by hour 24. This significant finding contributes to our understanding of the short-term effects of these mycotoxins on ogg1 genes in common carp hepatopancreas. One-year-old common carp juveniles were randomly distributed into five groups (Control, AFB1 0.4 mg kg-1 feed, STC1 1 mg kg-1 feed, STC2 2 mg kg-1 feed, and STC3 3 mg kg-1 feed). Hepatopancreas samples were collected three times (8, 16, and 24 h) in each group. No significant ogg1 and p53 expression changes were observed at 8 and 16 h after exposure. All measured genes were upregulated by the 24th hour in aflatoxin and STC3 groups. An increase in hsp70 gene expression was detected in all groups and all sampling. A significant decrease in gadd45aa gene expression was observed in the aflatoxin B1 group at hour 8. At hour 16, there was no significant change, while at hour 24, all treated groups were significantly different from the control. In summary, our results suggest that aflatoxin B1 and sterigmatocystin can stimulate the expression of DNA repair genes, mainly by hour 24. Further investigations are needed to get information about DNA damage parallel to the DNA repair mechanisms.

Exposure to a Combination of Fusarium Mycotoxins Leads to Lipid Peroxidation and Influences Antioxidant Defenses, Fatty Acid Composition of Phospholipids, and Renal Histology in Laying Hens.

The effects of combined short-term (3 days) exposure to Fusarium mycotoxins at both the EU recommended limit (T-2/HT-2 toxin: 0.25 mg/kg; DON/3-AcDON/15-AcDON: 5 mg/kg; FB1: 20 mg/kg) and twice the dose (T-2/HT-2 toxin: 0.5 mg/kg, DON/3-AcDON/15-AcDON: 10 mg/kg, and FB1: 40 mg/kg feed) on the kidneys of laying hens were examined. Our study aimed to investigate how these mycotoxins interacted with membrane lipid fatty acid (FA) composition and lipid peroxidation processes. It was observed that the levels of conjugated dienes and trienes were higher than the control in the low-mix group on day 3, and malondialdehyde concentration was higher on days 2 and 3. The proportion of phospholipid (PL) FAs showed that saturated and monounsaturated FAs increased. Still, both n3 and n6 polyunsaturated FAs decreased significantly on day 2 of exposure in the high-mix group. Among the n3 FAs, the level of docosahexaenoic (C22:6 n3) and among n6 FAs, arachidonic (C20:4 n6) acids decreased mainly on day 2 in the high-mix group. The results suggest that the combined exposure to Fusarium mycotoxins induced lipid peroxidation in the kidneys of laying hens, which resulted in marked changes in the PL FA profile. Histological examination revealed time- and dose-dependent increases as consequences of mycotoxin exposure.

The Effects of T-2 Toxin, Deoxynivalenol, and Fumonisin B1 on Oxidative Stress-Related Genes in the Kidneys of Laying Hens.

In the context of nephrotoxic risks associated with environmental contaminants, this study focused on the impact of mycotoxin exposure on the renal health of laying hens, with particular attention to oxidative stress pathways. Sixty laying hens were assigned to three groups-a control group (CON), a low-dose mycotoxin group (LOW), and a high-dose mycotoxin group (HIGH)-and monitored for 72 h. Mycotoxin contamination involved T-2/HT-2 toxin, DON/3-AcDON/15-AcDON, and FB1 at their EU-recommended levels (low mix) and at double doses (high mix). Clinical assessments revealed no signs of toxicity or notable weight changes. Analysis of the glutathione redox system parameters demonstrated that the reduced glutathione content was lower than that in the controls at 48 h and higher at 72 h. Glutathione peroxidase activity increased in response to mycotoxin exposure. In addition, the gene expression patterns of key redox-sensitive pathways, including Keap1-Nrf2-ARE and the AhR pathway, were examined. Notably, gene expression profiles revealed dynamic responses to mycotoxin exposure over time, underscoring the intricate interplay of redox-related mechanisms in the kidney. This study sheds light on the early effects of mycotoxin mixtures on laying hens' kidneys and their potential for oxidative stress.

The Effect of Combined Exposure of Fusarium Mycotoxins on Lipid Peroxidation, Antioxidant Defense, Fatty Acid Profile, and Histopathology in Laying Hens' Liver.

Fumonisin B1, T-2 toxin, and deoxynivalenol are frequently detected in feed materials. The mycotoxins induce free radical formation and, thereby, lipid peroxidation. The effects of mycotoxin exposure at the EU recommended limit (T-2/HT-2 toxin: 0.25 mg/kg; DON = 3AcDON/15-AScDON: 5 mg/kg; fumonisin B1: 20 mg/kg) and double dose (T-2/HT-2 toxin: 0.5 mg/kg, DON/3-AcDON/15-AcDON: 10 mg, and FB1: 40 mg/kg feed) were investigated during short-term (3 days) per os exposure in the liver of laying hens. On day 1 higher while on day 3 lower MDA concentrations were found in the low-dose group compared to the control. Fatty acid composition also changed: the proportion of monounsaturated fatty acids increased (p < 0.05) and the proportion of polyunsaturated fatty acids decreased by day 3. These alterations resulted in a decrease in the index of unsaturation and average fatty acid chain length. Histopathological alterations suggested that the incidence and severity of liver lesions were higher in the mycotoxin-treated laying hens, and the symptoms correlated with the fatty acid profile of total phospholipids. Overall, the findings revealed that mycotoxin exposure, even at the EU-recommended limits, induced lipid peroxidation in the liver, which led to changes in fatty acid composition, matched with tissue damage.

The Co-Occurrence of T-2 Toxin, Deoxynivalenol, and Fumonisin B1 Activated the Glutathione Redox System in the EU-Limiting Doses in Laying Hens.

Different mycotoxins in feed lead to combined exposure, increasing adverse effects on animal health. Trichothecene mycotoxins have been associated with inducing oxidative stress, which is neutralized by the glutathione system within the antioxidant defense, depending on the dose and duration of exposure. T-2 toxin, deoxynivalenol (DON), and fumonisin B1 (FB1) are commonly found in feed commodities simultaneously. In the present study, the intracellular biochemical and gene expression changes were investigated in the case of multi-mycotoxin exposure, focusing on certain elements of the glutathione redox system. In a short-term feeding trial, an in vivo study was performed with low (EU-proposed) doses: T-2/HT-2 toxin: 0.25 mg; DON/2-AcDON/15-AcDON.: 5 mg; FB1: 20 mg/kg feed, and high doses (twice the low dose) in laying hens. The multi-mycotoxin exposure affected the glutathione system; GSH concentration and GPx activity was higher in the liver in the low-dose group on day 1 compared to the control. Furthermore, the gene expression of antioxidant enzymes increased significantly on day 1 in both exposure levels compared to the control. The results suggest that when EU-limiting doses are applied, individual mycotoxins may have a synergistic effect in the induction of oxidative stress.

Fumonisin B Series Mycotoxins' Dose Dependent Effects on the Porcine Hepatic and Pulmonary Phospholipidome.

Male weaned piglets n = 6/group were fed Fumonisin B1+2+3 (FBs) mycotoxins at 0, 15, or 30 mg/kg diet for 3 weeks to assess the fatty acid (FA) composition of membrane lipid classes, lipid peroxidation, and histomorphological changes in the liver and lung. Growth performance and lipid peroxidation were unaltered, but histomorphological lesion scores increased in the liver. Linear dose-response was detected in liver phosphatidylcholines for C16:1n7, C18:1n9, and total monounsaturation and in lungs for C22:6n3, total n-3 and n-3:n-6, in pulmonary phosphatidylserines C20:0 and C24:0. Alterations associated with the highest FBs dose were detected in sphingomyelins (liver: total saturation ↓, total monounsaturation ↑), phosphatidylcholines (liver: total n-6 ↓, n-6:n-3 ↑; in lungs: total monounsaturation ↑, total polyunsaturation ↑), phosphatidylethanolamines (liver: total n-3 ↓; in lungs: total monounsaturation ↑ and n-6:n-3 ↑), phosphatidylserines (liver: n-6:n-3 ↑; in lungs: total saturation ↓, total polyunsatuartion ↑, and total n-6 and its ratio to n-3 ↑), and phosphatidylinositol (n-6:n-3 ↑; lungs: C22:1n9 ↑, C22:6n3 ↓, total saturation ↓, total monounsaturaion ↑). In conclusion, FBs exposures neither impaired growth nor induced substantial lipid peroxidation, but hepatotoxicity was proven with histopathological alterations at the applied exposure period and doses. FA results imply an enzymatic disturbance in FA metabolism, agreeing with earlier findings in rats.

Effect of diets with different inclusion levels of distillers dried grain with solubles combined with lysine and methionine supplementation on the lipid peroxidation and glutathione status of chickens.

To study the possible effects of different inclusion levels of distillers dried grain with solubles (DDGS) on the lipid peroxidation and glutathione redox status of chickens, 200 three-week-old Ross 308 cockerels were assigned to four treatment groups of 50 birds each. The groups were fed a control and three experimental, isocaloric and isonitrogenous grower diets containing 15, 20 and 25% DDGS, respectively, combined with lysine (Lys) and methionine (Met) supplementation until 6 weeks of age. It was found that DDGS inclusion increased the ether extract content of the diets which resulted in higher reduced glutathione (GSH) content and elevated glutathione peroxidase activity (GSHPx) in the liver. However, DDGS addition with Lys and Met supplementation did not influence the malondialdehyde content of the blood and the liver. The oleic acid proportion of the diet showed a close positive correlation with GSH content of the liver. A smaller ratio of methionine and cysteine in the diet with DDGS resulted in significantly higher liver GSH content. GSHPx activity increased parallel with the elevated GSH content of the liver homogenate, suggesting that the enzyme is activated by the actual supply of its co-substrate. In conclusion, the results show that DDGS, even at a high inclusion level combined with Lys and Met supplementation, has no initiative effect on lipid peroxidation in the blood and liver of broiler chickens.

The Effects of Mixed Fusarium Mycotoxins at EU-Permitted Feed Levels on Weaned Piglets' Tissue Lipids.

At exactly the individual permitted EU-tolerance dietary limits, fumonisins (FB: 5 mg/kg diet) and mixed fusariotoxins (DZ: 0.9 mg deoxynivalenol + 0.1 mg zearalenone/kg diet, and FDZ: 5 mg fumonisins + 0.9 mg deoxynivalenol + 0.1 mg zearalenone/kg diet) were administered to piglets (n = 6/group) for three weeks. Bodyweights of intoxicated piglets increased, while feed conversion ratios decreased. In FDZ, both the absolute and relative weight of the liver decreased. In the renal-cellular membrane, the most pronounced alterations were in FDZ treatment, followed by individual FB exposure. In both treatments, high proportions of C20:0 and C22:0 with low fatty acid (FA) unsaturation were found. In hepatocyte phospholipids, FDZ toxins exerted antagonistic interactions, and FB had the strongest increasing effect on FA monounsaturation. Among all investigated organs, the spleen lipids were the least responsive, in which FDZ expressed synergistic reactions on C20:0 (↑ FDZ vs. FB) and C22:0 (↓ FDZ vs. DZ). The antioxidant defense of the kidney was depleted (↓ glutathione concentration by FB-exposure). Blood plasma indicated renal injury (profound increase of urea and creatinine in FB vs. DZ and FDZ). FB strongly increased total-cholesterol and low density lipoprotein concentrations, whereas FDZ synergistically increased gamma-glutamyltransferase, alkaline-phosphatase, calcium and phosphorus levels. Summarized, individual and combined multiple fusariotoxins modified the membrane lipid profile and antioxidant defense of splanchnic organs, and serum biochemicals, without retarding growth in piglets.